Term
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Definition
| basic reaction or processes common to most tissues |
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Term
|
Definition
| specific responses or processes in specific organs or tissue |
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Term
| Acquired Causes of Cell Injury |
|
Definition
| hypoxia/ischemia, immunologic, physical, chemical, nutritional, infectious |
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Term
| Understanding morphological change is important for two reasons: |
|
Definition
1.) It helps us understand the underlying pathophysiology
2.) We can look at tissue morphology in order to decide how screwed a patient is. Or I mean, diagnose them or whatever. WHATEVER WE ARE PHARMACISTS. |
|
|
Term
| What are the most important types of changes that can cause lethal damage to the cell? |
|
Definition
| Intracellular increase of calcium, reduction of ATP, membrane permeability, oxygen |
|
|
Term
| Intrinsic Sources of Cell Injury |
|
Definition
| genetic derangements, which is how physiologists say mutations. And aging. |
|
|
Term
| How does cell damage cause symptomatic disease? |
|
Definition
| Cell damage causes symptomatic disease, because in order to survive the cell must adapt, and the adaptations can cause a reduction of function. |
|
|
Term
| What are some sites that are vulnerable to cell injury? |
|
Definition
| Cell membranes, aerobic respiration, protein synthesis and DNA integrity. |
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Term
| About how long does it take for an injured cell to undergo a morphological change? |
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Definition
|
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Term
| What parts of the cell can be damaged by too much calcium in a cell? |
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Definition
| Membrane, nuclear chromatic |
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Term
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Definition
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Term
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Definition
|
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Term
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Definition
| No oxygen because you ain't breathing. Like you tried to swallow one of those giant jaw breakers whole. Don't do that. |
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Term
|
Definition
| Decreased blood flow, leading to loss of oxygen and nutrients. Like when you wrap a rubber band around your finger until it turns white. Don't do that. |
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Term
|
Definition
|
|
Term
| Types of Cell Injury Due to ROS |
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Definition
| lipid peroxidation of membranes, oxidative modification of proteins (sulfhydryl cross-linking), DNA damage |
|
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Term
| What events happen as a result of cell damage, but don't indicated permanent cell damage? |
|
Definition
| Decreased respiration and loss of ATP•Glycogenolysis andg lycogen depletion•Reduction in intracellular pH (lactic acid)-Clumping of nuclear chromatin•Failure of membrane transport systems-Cellular edema (water accumulation due to increasein intracellular Na+)•Detachment of ribosomes and decreased protein synthesis |
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Term
| What are forms of irreversible cell injury? |
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Definition
| Massive influx of calcium•Membrane damage-Phospholipases-ROS•Intracellular release of lysosomal enzymes-RNAases, DNAases, proteases |
|
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Term
| What is the morphology of a reversible injury? |
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Definition
| -Cellular swelling (hydropic change)-Fatty change• |
|
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Term
| What is the morphology of an irreversible cell injury? |
|
Definition
| Autolysis or auto-digestion-Denaturation of cellular proteins |
|
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Term
| What is one way damage to midochondria can manifest? |
|
Definition
| Damage to mitochondria results in their taking up excess fluid and swelling |
|
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Term
| What causes fatty change in liver? |
|
Definition
| As the cells are damaged, lipid metabolism is altered and the liver becomes fatty. An especially common result of excessive ethanol intake, but occurs in other disease states as well. |
|
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Term
| What can cause kidney necrosis? |
|
Definition
| the blood supply was clogged by a small clot (thrombus), resulting in tissue death or necrosis. |
|
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Term
| Common early changes of necrosis? |
|
Definition
| •Hypereosinophilia (more red)•Cytoplasmic vacuolization•Nuclear changes-Pyknosis (shrunken and hyperchromic)-Karyorrhexis (fragmented)-Disappearance• |
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Term
|
Definition
|
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Term
|
Definition
| A type of necrosis that results from ischemia |
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Term
|
Definition
| Preservation of cell outlines and tissue structure-Prototype -myocardial infarction• |
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Term
|
Definition
| nsult leading to an influx of neutrophils releasing catalytic enzymes-Loss of cell outlines and tissue structure-Prototype -bacterial abscess• |
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Term
| Special Catagories of Necrosis |
|
Definition
| Caseous necrosis, enzymatic fat necrosis, and gangrene necrosis |
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Term
|
Definition
| Gross morphology of tissue is destroyed, but remains solid. Happens in TB |
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Term
|
Definition
| Essentially turns your pancrease to soap, because pancreatic enzymes break down fats and they form complexes p |
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Term
|
Definition
| CAn be caused by diabetic blood vessel disease |
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Term
|
Definition
|
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Term
|
Definition
| Programed cell death, Cell deletion in proliferating tissues-surface epithelium, immune system, tumors- Hormone-related involution-endometrium and breast-Response to specific types of injury-virus (hepatitis B & C), radiation and T-cell killing |
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Term
|
Definition
| Result of irreversible cell injury, passive. The lazy cell's apoptosis. |
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Term
| Morphology of a Dead and Dying Cell |
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Definition
| Progressin chromatin condensation, followed by nuclear and cellular fragmentation |
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Term
|
Definition
| Apoptosis of many of these lymphocytes, which manifest as small dark nuclear remnants inside semi-clear spaces that are macrophages. |
|
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Term
| What are some inducers of apoptosis? |
|
Definition
| Withdrawal of tropic factors like hormones or growth factors-Cytochrome C release from mitochondria inducescaspases (proteolytic enzymes)-Protein and DNA breakdown•Engagement of death receptors like Tumor Necrosis Factor receptor on cell-Ligand causes direct activation of caspases |
|
|
Term
| How is apoptosis regulated? |
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Definition
| Series of proteins that increase or inhibit apoptosis |
|
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Term
| How can lysosomes help cells adapt to injury? |
|
Definition
| Lysosomal degradation can occur, where lysosomes destroy the damaged organelles within a cell. |
|
|
Term
| What does smooth ER induction do to help a cell adapt to injury? |
|
Definition
| It helps a cell's ability to metabolize drugs and toxins. |
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Term
|
Definition
| More cells than normal, only in dividing cells, usually cells under hormonal control |
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Term
|
Definition
|
|
Term
| Does hypertrophy or hypersplasia occur in the prostate gland? |
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Definition
|
|
Term
| What is an example of GOOD hypertrophy? |
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Definition
| The cells in a pregnant uterus |
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|
Term
| What is an example of BAD hypertrophy? |
|
Definition
| Muscular dystrophy, the heart of people with hypertension |
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Term
|
Definition
|
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Term
|
Definition
|
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Term
|
Definition
| The substitution of one cell type for another, incorrect, cell type |
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Term
|
Definition
|
|
Term
| What is the earliest step of atherosclerosis? |
|
Definition
| Accumulation of cholesterol in macrophages. |
|
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Term
| Intracellular Accumulation Mechanisms |
|
Definition
| •Abnormal metabolism (fatty liver)•Abnormal protein folding (prion protein infection / mad cow disease)•Genetic enzymatic defect•Incomplete lysosome degradation |
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Term
|
Definition
| The area where the infection is and where phagocytosis and the killing of bacteria is taking place. |
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Term
|
Definition
| neutrophils infiltrate cell, takes place within a few minutes to hour after stimulus, usually transient. |
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Term
|
Definition
|
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Term
|
Definition
| The process of a cell being attracted to move towards a certain stimulus. Sometimes products from a bacteria. |
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Term
|
Definition
| Persistence of injurious agent in a way that interferes with the healing process leads to chronic inflammation. |
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Term
|
Definition
| A series of plasma proteins with proteolytic activity that are activated by contact with the bacterial surface and sequentially activate successive members of the cascade. |
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Term
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Definition
|
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Term
|
Definition
| Scarring, leading to impaired function. |
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Term
|
Definition
| Migration of fibroblasts to deposit extracellular matrix (mostly collagen) |
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Term
|
Definition
| Connective tissue containing rapidly proliferating blood vessels and fibroblasts and usually some inflammatory cells. |
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Term
|
Definition
| An intense form of chronic inflammation that is most often associated with TB |
|
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Term
|
Definition
| transmembrane heterodimers important in cell-cell and cell-ECM interactions, named by their β chains, or sometimes a common nam |
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Term
|
Definition
| Antigen specific leukocyte, T and B |
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Term
|
Definition
|
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Term
|
Definition
|
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Term
|
Definition
| Phagocytose bacteria, dead cells and debris. They are part of the innate immune system. |
|
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Term
|
Definition
| the binding of a substance to the surface of a bacteria or other antigen and increases its uptake by neutrophils or macrophages. |
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Term
|
Definition
| Clearing of the infection |
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Term
|
Definition
| L-selectin mediates an important step in leukocyte adhesion in inflammation. |
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Term
|
Definition
| The various outcomes and processes associated with healing damage and/or clearing a bacterial infection. |
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|
Term
| Transendothelial Migration |
|
Definition
| The movement of things through the endothelium |
|
|
Term
| What is inflammation supposed to do for the body? |
|
Definition
|
|
Term
| What are some gross (like macro, not like yucky, but maybe yucky) signs of inflammation? |
|
Definition
| Firm, tender and swollen (edema). Red and warm to the touch (from increased blood flow) |
|
|
Term
| What is a hallmark of inflammation? |
|
Definition
| Infiltration of the tissue with any of the classes of leukocytes, neutrophils in acute inflammation, lymphocytes and monocytes in chronic inflammation. |
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|
Term
| What is probably the single most important host defense against infectious disease? |
|
Definition
| Phagocytosis and killing of microorganisms |
|
|
Term
| How can you determine, by looking at the nucleus, if a cell is a neutrophil? |
|
Definition
| It has a multi-lobed nucleus |
|
|
Term
| What are the steps in acute inflammation? |
|
Definition
| 1.) increased blood flow 2.) extravasation and deposit of fluid and plasma proteins. 3.) emigration of neutrophils from the microcircualtion and their accumulation at the site of injury. |
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Term
|
Definition
| Increased pressure in the capillary bed and changes in the vessel itself |
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|
Term
| Endothelial cell retraction |
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Definition
| Acompanies acute and some chronic inflammation. Allows for increased permeability |
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Term
|
Definition
| Area of nasopharyngeal mucosa that has a lot of edema, due to an allergic response. The more usual neutrophil-rich acute inflammatory responses are also edematous, but much less so than these allergy responses. |
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Term
| Regulators of Vascular Permeability |
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Definition
|
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Term
|
Definition
| -Secreted by mast cells, present in most tissues-Release causes vasodilatation of arterioles andincreased permeability in venules-Results in fluid leak-Especially prominent role in allergic response,causing edema (as in the nasal polyp) |
|
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Term
|
Definition
| -In circulating platelets-Activity similar to that of histamines |
|
|
Term
| The complements responsible for vasodilation and permeability? |
|
Definition
|
|
Term
| Which complement is a powerful chemotactic agent for neutrophils? |
|
Definition
|
|
Term
| Which complements act as opsonins? |
|
Definition
|
|
Term
| What are the characteristics of chronic inflammation? |
|
Definition
| -monocute and lymphocyte infiltration, takes about 24hrs for maximum infiltration, persists for weeks or more, many functions, often due to immune response |
|
|
Term
| How do leukocytes exit the blood stream? |
|
Definition
| By passing through the walls of small venules |
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Term
|
Definition
| initial adhesive interaction with the endothelium; cell slows down but does not completely stop. |
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Term
|
Definition
| leukocytes literally roll across the surface of the endothelium. The cells stop only after they are triggered to adhere firmly. See the movie to see this process |
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Term
|
Definition
|
|
Term
| Where are integrins expressed? |
|
Definition
|
|
Term
|
Definition
| ECM proteins and also Bind to counter receptors induced on activated endothelial cells at sites of inflammation: |
|
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Term
| What are a couple of examples of integrin-counter receptor binding pairs? |
|
Definition
-Mac-1 on neutrophils & monocytes to ICAM-1 on EC
-LFA-1 on lymphocytes to ICAM-1 on EC |
|
|
Term
| What superinduces InterCellular Adhesion Molecule-1 (ICAM-1)? |
|
Definition
| Cytokines released locally by lymphocytes and tissue macrophages. |
|
|
Term
| What does the L in L-selectin stand for? |
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Definition
|
|
Term
| How do selectins bind to counterreceptors? |
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Definition
| Via n-terminal lectin domains to CHO groups on the counter receptors. |
|
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Term
|
Definition
| constitutively by monocytes, neutrophils and most lymphocytes |
|
|
Term
| What does L-selectin mediate adhesion to? |
|
Definition
| ligands induced on endothelial cells at sites of inflammation |
|
|
Term
| What up-regulates adhesive function in integrins? |
|
Definition
|
|
Term
| Features of Selectin-Mediated Adhesion |
|
Definition
| Very rapid 0n-rate, loose interactions, rolling interactions with endothelium |
|
|
Term
| Initial adhesive interaction: |
|
Definition
| L-selectin with its endothelial ligand. This loose interaction slows the cell down, but cannot completely stop it. Results in rolling of the leukocyte across the endothelial surface. |
|
|
Term
| What causes firm adhesion? |
|
Definition
| The high affinity binding of mac-1 to ICAM-1 |
|
|
Term
| Outcomes of Acute Inflammation |
|
Definition
| •Complete resolution -no permanent damage; regain function (e.g., pneumococcal pneumonia)•Healingbytissue replacement (fibrosis)•Chronic inflammation-persistence of injurious agent, interference with healing process-Common in autoimmune diseases |
|
|
Term
| What is the major regulatory molecule of angiogenesis? |
|
Definition
|
|
Term
|
Definition
| Capillary budding, endothelial cell proliferation |
|
|
Term
| Major stimulatory molecule in Fibrogenesis? |
|
Definition
|
|
Term
| What are the barriers meant to prevent infectious diseases from coming into contact with your immune system in the first place? |
|
Definition
| Mechanical, biochemical, and microbiological |
|
|
Term
| Rapid (Innate) Immune Response |
|
Definition
| Involves pathogen recognition and destruction and causes inflammation at the site of the attack |
|
|
Term
| Slow (Adaptive) Immune Response |
|
Definition
| Adds focus and power to the innate immune response. Unlike innate: 1. Is slower but more variable in scope.2. Exhibits numerous, highly selectivespecificities.3. Improves during the response.4. Produces immunologic memory |
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Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Acidity (GI and urogenital tracts) •Antimicrobial peptides called “defensins”•Skin: Sebum•GI tract: Proteases•Lysozyme in nasal secretions and tears•Spermine and zinc in semen |
|
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Term
|
Definition
| Epithelial cells joined by tight junctions•Sloughing off epithelial layers•Flow of fluids (sweat, tears, saliva, urine, sperm) or mucus |
|
|
Term
| What cells do all immune cells derive from? |
|
Definition
|
|
Term
| Immune Cells that are key in innate immune response |
|
Definition
| Monocytes and neutrophils, macrophages and NK cells. |
|
|
Term
| Immune cells that are key in adaptive immune response |
|
Definition
| Lymophocytes (B and T cells) |
|
|
Term
| Which cells link the innate and adaptive immune responses? |
|
Definition
| Dendritic Cells and macrophages |
|
|
Term
| Describes the steps in the innate immune pathway: |
|
Definition
| Complement fragment binds to the outside of the bacterial cell, which is recognized by a receptor on the leukocyte (neutrophil, macrophage, monocyte or NK cell) which then engulfs the cell and KILLS IT. |
|
|
Term
| What are the cells of the adaptive immune system? |
|
Definition
|
|
Term
| Where do T- and B-lymphocytes develop and reside? |
|
Definition
| Bone marrow and thymus are primarylymphoid tissues. Lymph nodes, spleen, Peyer’s patches, appendix, tonsils etc are secondary lymphoid tissues. |
|
|
Term
| Where are T-lymphocytes typically developed? |
|
Definition
|
|
Term
| Where are B-lymphocytes developed? |
|
Definition
| Bone Marrow, with final maturation in the spell |
|
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Term
|
Definition
| Mucosa Associated Lymph tissue is a secondary lymphoid tissue that communicates with the microflora in the GI, respiratory and urogenital tracts as well as all other mucosal surfaces. |
|
|
Term
|
Definition
| Contain a heavy chain and a light chain |
|
|
Term
|
Definition
| Have an alpha and beta chain |
|
|
Term
| What is the principle effector mechanism of humoral immunity (the B-cell response)? |
|
Definition
| Antibody (secreted immunoglobulin) |
|
|
Term
| Which T-Cell turns into a Killer Cell? |
|
Definition
|
|
Term
| What types of cells do CD4+ cells differentiate into? |
|
Definition
| Helper and Regulatory T-Cells |
|
|
Term
| How long does it take for the innate immune response to start after an infection has overcome the barriers? |
|
Definition
|
|
Term
| How long does it take for the innate immune response to shift from ubiquitous to induced? |
|
Definition
|
|
Term
| What leads to AIDS in HIV infected people? |
|
Definition
| Gradual extinction of helper T-Cells |
|
|
Term
| What are the ways that HIV leads to T-Cell extinction? |
|
Definition
| cytopathic effect of virus itself, HIV-specific cytotoxic T cells kill cells that are infected, uninfected cells undergo apoptosis. |
|
|
Term
| What are malignancies associated with HIV? |
|
Definition
| KAposi's sarcoma, Non-hodgekin's lymphoma |
|
|
Term
| What inherited immune diseases are caused by a defect in macrophages? |
|
Definition
| Chronic Granulomatous, Glucose-6-phosphate dehydrogenase deficiency |
|
|
Term
| What inhereited diseases are caused by a defect in Neutrophils? |
|
Definition
| Leukocyte adhesion deficiency (Caused by lack of CD18= beta 2 integrin), MPO deficiency |
|
|
Term
| What are two examples of X-linked immunodeficiency diseases? |
|
Definition
| XLA and X-linked hyper IgM syndrome |
|
|
Term
| What are four diseases caused mainly by dysfunctional T-lymphocytes? |
|
Definition
| X-linked SCID [due to lack of common cytokine receptor γchain]•Wiskott-Aldrich syndrome [WAS, X-linked]•Bare lymphocyte syndrome [lack of MHC class II on antigen-presenting cells•ADA (adenosine deaminase) or PNP purine nucleotide phosphorylase deficiencies |
|
|
Term
| Diseases due to defects in the genetic B-Cell and T-cell receptor assembly |
|
Definition
| RAG deficiency[no B cells and T cells]•Omenn syndrome [weak efficiency allele of RAG]•Artemis [defective DNA doublestrand break repair ] |
|
|
Term
| What are the two types of pathologic immune responses? |
|
Definition
| Exaggerated response and autoimmune response |
|
|
Term
| What are the immunopathologic mechanisms: |
|
Definition
• Antibody-mediated (B lymphocytes)
• Type I. Anaphylactic/atopic mechanism (Immediate)
• Type II. Opsonization/Cellular dysfunction mechanism (Antibody mediated)
• Type III. Immune-complex mechanism (Immune complex mediated)
• Cell-mediated (T lymphocytes, histiocytes)
• Type IV. Delayed hypersensitivity mechanism (Cell mediated) |
|
|
Term
| What is the Type I immunopathologic mechanism? |
|
Definition
| Anaphylaxis, IgE binds to mast cells and basophils. Immediate histamine release, vasodilation and leakage, more mucus, eosinophil infiltration and vascular collapse. If person survivives, synthesis and release ofleukotrienes, prostaglandins |
|
|
Term
| What is the Type II mechanism? |
|
Definition
| Opsonization/Cellular disfunction |
|
|
Term
| Explain the cytotoxic form of the type II mechanism? |
|
Definition
Cytotoxic
• Antibodies bind to cell surface molecules and fix complement
• Two cytotoxic mechanisms.
-Complement may lyse cells on its own.
-Bound antibody and complement direct an immune response at the cell. |
|
|
Term
| Explain the non-cytotoxic form of the type II mechanism? |
|
Definition
• These reactions are against cell surface and extracellular matrix antigens
• Antibodies to structural proteins
• Antibodies against cell receptors can activate or inactivate a cellular function |
|
|
Term
|
Definition
| ↑Thyroid hormone (T3, T4) secretion→hypermetabolic state: heat intolerance, weight loss, hyperreflexia, protruding eyes. |
|
|
Term
|
Definition
| Skeletal muscle acetyl choline receptors are blocked or bound by antibody →blocking of the neuronal impulse transmission across neuron-muscular junction→muscle weakness. |
|
|
Term
What are the two mechanis of TYPE III
Immune Complex Diseases? |
|
Definition
Antibodies form vs foreign or self antigens either in 1.)circulation or 2) localized in tissue (2) or localized in tissue
Complement system (C’) activation → ↑ vascular permeability + chemotactic & opsonic C’ fragments that ↑activity of PMNs → Tissue PMN infiltrate & ↑phagocytosis. → Local destruction of blood vessels and connective tissue.) |
|
|
Term
| Clinical features of systemic immune complex diseases: |
|
Definition
• Fever
• Urticaria (itchy, swollen areas of skin)
• Arthralgias (joint pain)
• Proteinuria and hematuria (glomerular injury)
• Lymphadenopathy (swollen lymph nodes) |
|
|
Term
| Examples of immune complex mediated diseases |
|
Definition
• Systemic lupus erythematosus.
• Rheumatoid arthritis.
• Glomerulonephritis (renal injury) of several etiologies. |
|
|
Term
Explain the two types of Type IV
Delayed hypersensitivity and T cell-mediated cytotoxicity: |
|
Definition
Two types:
Cell-mediated cytotoxicity: Mediated by T8+ T cells. Example: Poison ivy dermatitis.Granulomatous reactions Examples: TB skin test reaction, TB, fungal infections. |
|
|
Term
| Two major categories of autoimmune disease |
|
Definition
Systemic (multi-organ) diseases.
• Examples: Systemic Lupus Erythematosus, rheumatoid arthritis, Wegener’s Granulomatosis and other types of systemic vasculitis
Organ-system or cell-type specific diseases.
• Examples: Grave’s disease, Hashimoto’s thyroiditis, myasthenia, pemphigus. |
|
|
Term
| What is the patient population of systemic lupus erythematosis? |
|
Definition
| mostly female (10:1) , of childbearing age. |
|
|
Term
| What is the prevalence of SLE? |
|
Definition
|
|
Term
|
Definition
| Yes. Linked to certain HLA types, especially DR2 and DR3. Also associated with a congenital deficiency of C2 and C4. |
|
|
Term
| What are the recognized subtypes of SLE? |
|
Definition
| Chronic Discoid Lupus, Subacute Cutaneous Lupus and drug induced lupus |
|
|
Term
|
Definition
| Yes. Linked to certain HLA types, especially DR2 and DR3. Also associated with a congenital deficiency of C2 and C4. |
|
|
Term
| What are the symptoms of chronic discoid lupus? |
|
Definition
| skin manifestations only, usually on the face and scalp, red scaly plaques, systemic manifestations only occur in 5-10% of the population |
|
|
Term
|
Definition
| Widespread skin rash and mild systematic systems. Associated with anti-SSA and HLA-DR3 genotype. |
|
|
Term
|
Definition
• A lupus like syndrome caused by drugs which induce ANA formation
• (e.g Procainamide, hydralazine, isoniazid, Penicillamine)
• Typically these patients do not get CNS or renal manifestation, unlike normal lupus
• Ant- DS-DNA antibody negative
• Anti-histone antibody positive
• Patients with HLA-DR4 are more susceptible follow hydralazine administration
• Goes away when you take away the drug. |
|
|
Term
| What are the diagnostically important antibodies in SLE? |
|
Definition
• ANA (AntiNuclear Antibodies): Present in more than 95% of SLE pts.
• Anti-native DNA (also called anti-double stranded DNA)
• Anti-Sm (Anti-Smith) |
|
|
Term
|
Definition
| Change behavior, avoid sun, immuno-suppressants as necessary. |
|
|
Term
| What is the patient population of rheumatoid arthritis? |
|
Definition
| 1-3% of adults, 3X more women than men, primarily 35-50y/os |
|
|
Term
| What are the symptoms of RA? |
|
Definition
• Typically involves 2-3 symetric joints
• Pain, particularly in the morning
• Stiffness
• Swelling
• Inflammation
• Generalized immune symptoms
• Malaise, fever, fatigue, loss of appetite, weight loss, myalgias,weakness
• Long duration: > 6months
• Symmetrical deforming arthritis which affects multiple joints; especially hands & wrists.
• Disease is of variable severity; severe cases often have systemic symptoms.
• Pediatric or “Juvenile RA” less common but more severe than adult form. |
|
|
Term
| Etiology and Pathogenesis of RA: |
|
Definition
• Initiating events are unknown. Infiltrating leukocytes and inflamed synovial cells secrete TNFα (tumor necrosis factor). This causes inflammation of joint cartilage and bone and sets up a positive feedback loop perpetuating joint inflammation & injury.
• Both humoral (Hypersensitivity reactions II & III) and cell-mediated immunity (IV) are involved in joint pathology. Type III mechanisms are involved in extra-articular manifestations. |
|
|
Term
| Diagnostically important Antibodies in RA: |
|
Definition
| Rheumatoid factor, an autoantibody against denatured self-IgG is detected in the serum of 80% of R.A. In the appropriate clinical context, it is a useful screening test, although not specific to R.A. |
|
|
Term
| Sjogren's (sicca) syndrome |
|
Definition
| salivary and lacrimal gland destruction → dry mouth, dry eyes |
|
|
Term
|
Definition
| Both skin and skeletal muscle damage |
|
|
Term
|
Definition
| skeletal muscle inflammation and destruction → muscle atrophy |
|
|
Term
|
Definition
| Wide-spread progressive fibrosis in skin and visceral organs |
|
|
Term
|
Definition
| involves skin and connective tissue, benign |
|
|
Term
|
Definition
| some patients have "mixed" syndromes |
|
|
Term
| Autoimmune (Hashimoto's) thyroiditis patient population: |
|
Definition
| Adult females 10-20X more common than men |
|
|
Term
| Symptoms of Hashimoto's Thyroiditis |
|
Definition
| Swollen neck due to variable enlargement of the thyroid gland. Patient may be euthyroid, hyperthyroid or hypothyroid at different stages of disease. |
|
|
Term
|
Definition
Thyroid gland is infiltrated by both B and T lymphocytes; and slowly becomes hypotrophic as glandular epithelium is destroyed and replaced by fibrous tissue.
• Immunopathologic mechanisms - Type II cytotoxicity is involved; also possibly Type IV cell-mediated cytotoxicity |
|
|
Term
| Diagnostically important antibodies in thyroiditis? |
|
Definition
| Autoantibodies to thyroid antigens (mainly thyroid peroxidase) are present in ~ 95% of patients |
|
|
Term
| Clinical Course for Thyroiditis? |
|
Definition
• Hypothyroidism develops slowly.
• Patients will eventually require thyroid hormone. |
|
|
Term
| Diabetes mellitus (type 1) |
|
Definition
| Islet cell injury by autoantibodies and T cell cytotoxicity. |
|
|
Term
|
Definition
| due to anti-adrenal cortical cell abs. |
|
|
Term
| Multiple endocrine autoimmunity |
|
Definition
| Hereditary disease in which autoantibodies develop against several endocrine gland |
|
|
Term
| What kinds of cells do cancers usually arise from? |
|
Definition
|
|
Term
| What is an example of a negative feedback loop? |
|
Definition
| Gastrin secreting cells in the human stomach |
|
|
Term
| What is a characteristic of neoplasia (especially malignancy)? |
|
Definition
| Genomic instability. It is a positive feedback loop. |
|
|
Term
| Cancer is a Genetic Disease |
|
Definition
| Tumors are being selected for. |
|
|
Term
|
Definition
| Lines everything, secretes, lubricates absorbed, a-vascular. |
|
|
Term
| Why do epithelia lead to cancer? |
|
Definition
| Large surface area, more area to be exposed to cancer. |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Benign tumors of the squamous epithelium |
|
Definition
|
|
Term
| Malignant tumors of the squamous epithelium |
|
Definition
|
|
Term
| MAlignant Haemopoetic tumors |
|
Definition
|
|
Term
| Malignant Melanocytes tumors |
|
Definition
|
|
Term
| Malignant Germ Cell tumors |
|
Definition
| Seminoma Yolk sac tumor Embryonal carcinoma Choriocarcinoma |
|
|
Term
| Benign Melanocytes tumors |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Derived from a single cell |
|
|
Term
|
Definition
|
|
Term
| The decreased incidence of what sort of bacteria has lead to a decreased incidence of GI cancer? |
|
Definition
|
|
Term
| The advent of what test has lead to a decreased incidence of cervical cancer? |
|
Definition
|
|
Term
| Who started smoking later and less, and have continued smoking for longer? |
|
Definition
|
|
Term
| For which type of cancer does age play a bigger role? |
|
Definition
|
|
Term
| Classes of genes altered in cancer– |
|
Definition
| •Classes of genes altered in cancer–Oncogenes (growth promoting)•Activating mutation, translocation, amplification–Tumor suppressor genes (growth-inhibiting)•Inactivating mutation, deletion, methylation –Genes that regulate apoptosis (programmed cell death)–Genes involved in DNA repair |
|
|
Term
| What's an example of how cancers have self-sufficiency in growth signals? |
|
Definition
| Activating mutation leads to “locked on” KRAS |
|
|
Term
| What does the loss of RB lead to? |
|
Definition
| Uncontrolled transcription of growth promoting genes |
|
|
Term
| What happens when when growth inhibitory signals fail? |
|
Definition
| •Loss of p53 •No cell cycle arrest•No repair•No exit from cell cycle•No apoptosis |
|
|
Term
| What is one way a cell evades apoptosis? |
|
Definition
| Translocation of BCL-2 to IgH promoter |
|
|
Term
| What is another way a cell evades apoptosis? |
|
Definition
|
|
Term
| What is the sequence of events in cancer? |
|
Definition
| 1.Self-sufficiency in growth signals 2.Insensitivity to growth-inhibitory signals 3.Evasion of Apoptosis 4.Limitless replicative potential 5.Development of sustained angiogenesis 6.Ability to invade and metastasize 7.Genomic instability due to defects in DNA repair |
|
|
Term
| What are the three types of carcinogens? |
|
Definition
| Chemical, Radiation and virus or microbial |
|
|
Term
|
Definition
| Oncogenes E6 and E7 inactivate p53 and RB, respectively. |
|
|
Term
|
Definition
| Based on microscopic features and Refers to how well or poorly a tumor resembles the normal cells it recapitulates. |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| TNM Classification refers to: |
|
Definition
| Anatomic extent of the disease. |
|
|
Term
| TNM Classification is assigned: |
|
Definition
| At diagnosis. It is the most powerful predictor of outcome. |
|
|
Term
| Local signs and symptoms of cancer |
|
Definition
| swelling, ulceration, hemorrhage and pain |
|
|
Term
| signs and symptoms of metastatic cancer: |
|
Definition
| enlarged lymph nodes, splenomegaly, hepatomegaly, fracture of affected bones, neurological symptoms |
|
|
Term
| signs and symptoms of systemic cancer: |
|
Definition
| weight loss(poor appetiteand cachexia), fatigue, anemia(low red blood cell count) and other specific conditions termed paraneoplastic phenomena |
|
|
Term
|
Definition
Surgery
•Chemotherapy, hormonal therapy, immunotherapy
•Radiation Therapy |
|
|
Term
| How does cancer cause morbidity and mortality? |
|
Definition
| may replace and or destroy vital organs, leading to organ failure, compression of vital organs, rupture into major vessels, structures, cachexia, immunocompromise |
|
|
Term
| What social issues will arise as a result of genetic analysis being easier to preform? |
|
Definition
–Privacy
–Discrimination: •Jobs •Insurance |
|
|
Term
| Categories of genetic diseases |
|
Definition
| •Chromosomal disorders•Monogenetic disorders (Medelian)•Multifactorial disorders |
|
|
Term
| What are the steps of cytogenic analysis? |
|
Definition
| 1.) culture blood lymphocytes 2.) arrest at metaphase with colchicin 3.) lyse arrested cells on a glass slide 4.) stain chromosomes 5.) view chromosomes by microscope |
|
|
Term
| Can stored, frozen or formalin fixed tissues be used for cytogenetic analysis? |
|
Definition
|
|
Term
| What are some cell sources for cytogenetic analysis? |
|
Definition
| buccal scraping, biopsy material, white blood cells, amniotic cells |
|
|
Term
| Symptoms of down syndrome |
|
Definition
| Growth failure, mental retardation, flat occiput, congenital heart disease, slanted eyes, epicanthal fold, brushfield spots, dysplastic ears, protruding big, wrinkled tongue, short broad hands with almian crease, acute lymphoblastic leukemia, wide gap between 1st and 2nd toes. |
|
|
Term
| What's the most common sort of Down Syndrom |
|
Definition
|
|
Term
| Which kind of Down Syndrome has a high rate of recurrence and is responsible for ~4% of all cases of down syndrome? |
|
Definition
|
|
Term
| Which type of downs occurs early in embryo? |
|
Definition
|
|
Term
| Massively parallel sequencing methods are allowing for the sequencing of what type of DNA in order to predict whether or not a developing fetus has DS? |
|
Definition
| cell free fetal DNA (cffDNA) present in maternal plasma |
|
|
Term
|
Definition
| Only one X chromosome active, other is barr body. Inactivation is early in the embryo and is random. |
|
|
Term
|
Definition
| XXY, testical atrophy, tall, slim stature, gynecomastia, appearance of barr body |
|
|
Term
| Which disease results in female phenotype and zero barr bodies? |
|
Definition
|
|
Term
| Which disease results in female phenotype and 2 barr bodies? |
|
Definition
|
|
Term
| Which disease results in male phenotype and 1 barr bodies? |
|
Definition
|
|
Term
| Which disease results in male phenotype and e barr bodies? |
|
Definition
|
|
Term
| What are some examples of autosomal dominant diseases? |
|
Definition
| familial hypercholesterolemia, polycystic kidney disease, Huntington's disease, Marfan's syndrome |
|
|
Term
| What are some examples of autosomal recessive diseases? |
|
Definition
| Sickle cell anemia, cystic fibrosis, Tay-Sachs disease, Phenylketonuria |
|
|
Term
| What are some examples of X linked diseases? |
|
Definition
| Duchenne muscular dystrophy, hemophilia |
|
|
Term
| Consequences of single gene defects: |
|
Definition
Enzyme defects
•Membrane receptor defects
•Altered non-enzymatic proteins
•May be dominant or recessive |
|
|
Term
| What causes most of the morbidity in CF? |
|
Definition
|
|
Term
| What is the most common gene deletion that causes Cystic fibrosis? |
|
Definition
|
|
Term
| In what way is cancer a genetic disease? |
|
Definition
| •Neoplasms all contain multiple somatic mutations •No single mutation is sufficient to yield a malignant phenotype •A limited number (5-7?) rate limiting mutations are need to produce a cancer |
|
|
Term
| What disease does Neuorfibromin 1 cause? |
|
Definition
|
|
Term
| What disease does RB gene cause? |
|
Definition
|
|
Term
| What disease does p53 gene cause? |
|
Definition
|
|
Term
| What disease does APC gene cause? |
|
Definition
| Familial adenomatosis and colon CA |
|
|
Term
|
Definition
|
|
Term
| What disease do MEN1 and RET cause? |
|
Definition
| Multiple endocrine neoplasia 1 and 2 |
|
|
Term
| Neurofibromatosis symptoms |
|
Definition
| Familial tumor syndrome•Associated with germline loss of oneNeurofibromin 1 allele•Tumors exhibit loss of heterozygosityfor Neurofibromin 1•Tumors also contain additional somatic mutations |
|
|
Term
| Neurofibromatosis incidence |
|
Definition
|
|
Term
| Neurofibromatosis associated with germline loss of? |
|
Definition
| One neurofibromin1 allele |
|
|
Term
| What percentage of Neurofibromatosis cases arise spontaneously? |
|
Definition
|
|
Term
| What kind of inheritance do Familial cancer syndromes have? |
|
Definition
|
|
Term
| What are Familial cancer syndromes associated with? |
|
Definition
| Associated with mutations of tumor supressor or DNA repair/Genome maintenance genes• |
|
|
Term
| Familiar cancer syndromes have tissues that contain both normal and mutated genes... what happens in tumors? |
|
Definition
| Tumors have loss of heterozygosity due to somatic mutations |
|
|
Term
| Multifactorial inheritance are determined by... |
|
Definition
| a combination of genetic and environmental factors |
|
|
Term
| Multifactorial inheritance is responsible for many common disorders not limited to: |
|
Definition
| –Single congenital malformations–Diabetes, psychiatric diseases, hypertension |
|
|
Term
| The threshold effect of multifactorial inheritance refers to: |
|
Definition
| the observation that a minimum number of factors may be required for expression of a trait. |
|
|
Term
|
Definition
| improper fusion of embryonic structures leading to upper lip |
|
|
Term
| What is the risk of cleft palate in subsequent births? |
|
Definition
|
|
Term
| What is often the inciting cause of cleft palate? |
|
Definition
| OFten, there is no known inciting cause. |
|
|
Term
| What infections causes esophagitis? |
|
Definition
|
|
Term
| What is Eosinophilic esophagitis caused by? |
|
Definition
| Allergic reaction to foodstuffs |
|
|
Term
| What is the most common cause of esophagitis? |
|
Definition
|
|
Term
| What food item do the pseudohyphae of candida look like? |
|
Definition
|
|
Term
| What do CMV and herpes show? |
|
Definition
| Characteristic nuclear inclusions |
|
|
Term
| Which pathogen that causes esophogitis can have cytoplasmic inclusions? |
|
Definition
|
|
Term
| How can you treat eosinophilic esophagitis? |
|
Definition
| By removing the food or by using swallowed steroids and some asthma drugs. |
|
|
Term
| What are some causes of lower esophageal sphincter failure? |
|
Definition
| 1. ↑intra-abdominal pressure: -Lifting, obesity, pregnancy2. Direct injury:-Alcohol, tobacco3. From some foodstuffs |
|
|
Term
| In what condition is the squamous mucosa of the esophogus replaced by a glandular, Goblet-cell containing, mucosa |
|
Definition
|
|
Term
| Barrett's metaplasia leads to what kind of cancer? |
|
Definition
|
|
Term
| In US populations, squamous carcinoma is related to what? |
|
Definition
| alcohol and tobacco abuse |
|
|
Term
| Acute Gastritis is caused by and is characteristic of: |
|
Definition
| Alcohol and aspirin in large amounts, Usually severely hemorrhagic and life-threatening |
|
|
Term
| Chronic Gastritis is caused by: |
|
Definition
–Chemical gastropathy
–Autoimmune –“Pernicious anemia”
–Helicobacter pylori–Common!–Predisposes to ulcers–Predisposes to carcinoma and lymphoma |
|
|
Term
| Reactive (Chemical) Gastropathy, which can result in ulcers, is due to |
|
Definition
| Drugs (NSAIDs), and Bile reflux |
|
|
Term
| Autoimmune gastritis, caused by auto-immune antibodies attacking parietal cells in the gastric body and fundus can lead to: |
|
Definition
| –Loss of stomach acid–Loss of intrinsic factor (leads to B12 deficiency “pernicious anemia”) and an increased risk of neuroendocrine tumors and carcinomas |
|
|
Term
| Dense chronic inflammation in superficial mucosa is |
|
Definition
|
|
Term
| H. pylori is a major player in |
|
Definition
| Gastritis, peptic ulcer disease, and gastric carcinoma and gastric lymphoma |
|
|
Term
| How are gastric ulcers treated now? |
|
Definition
| Patients are treated with proton pump inhibitors and heliobacter organisms are eradicated |
|
|
Term
| What are complications of ulcers? |
|
Definition
| bleeding, perforation, obstruction and intractable pain. |
|
|
Term
|
Definition
| coffee ground colored vomit that indicates bleeding from an upper GI site |
|
|
Term
|
Definition
| dark, tarry stools, indicative of upper GI bleeding |
|
|
Term
| Bright red blood in stool |
|
Definition
| lower GI bleeding, caused by colon adenoma, colon cancer, hemorrhoids and others |
|
|
Term
|
Definition
| identified only when tested for chemically. |
|
|
Term
| With gastric adenocarcinoma, Early (before invasion goes beyond submucosa) detection is the difference between a 90% survival rate and a 15% survival rate... What % of cases are detected early? |
|
Definition
|
|
Term
|
Definition
| Pancreatic enzymes break down carbohydrates and proteins •Bile and lipase break down fat droplets• |
|
|
Term
|
Definition
| •Carbohydrate and protein molecules absorbed across epithelial layer•Fatty acids and monoglycerides directly diffuse across membrane |
|
|
Term
| What can cause maldigestion? |
|
Definition
| pancreatic insufficiency or alteration in the production or flow of bile |
|
|
Term
| Malabsorbtion is caused by |
|
Definition
| Small intestinal damage due to •Celiac disease•Giardia•Bacterial overgrowth•Tropical sprue•Whipple’s disease |
|
|
Term
| Celiac Diseasea is present in at least ___ of caucasions of european ancestry |
|
Definition
|
|
Term
| Celiac disease, which causes damage to the small intestine, is caused by |
|
Definition
| •Genetic predisposition + immune-mediated damage triggered by the ingestion of gluten (wheat, rye, or barley)•Association with other autoimmune diseases |
|
|
Term
| How can celiac disease be diagnosed by serological methods? |
|
Definition
| •IgA to tissue transglutaminase (TTG)•IgA or IgG antibodies to deamidated gliadin•Anti-endomysial antibodies |
|
|
Term
| Which parts of the GI system are most affected by Celiac disease? |
|
Definition
| Duodenum and proximal jejunum |
|
|
Term
| What are two key findings to diagnose Celiac disease? |
|
Definition
| increased intraepithial lymphocytes, then leter crypt hyperplasia and villous artrophy |
|
|
Term
| What is it that leads to malabsorption in Celiac disease? |
|
Definition
| Loss of mucosal and brush border surface area |
|
|
Term
| Infectious Enterocolitis causes how many deaths a day in children in developing countries? |
|
Definition
|
|
Term
| What Causes Infectious Enterocolitis? |
|
Definition
| LONGlist of potential oganisms:–Viral –rotovirus, norovirus, adenovirus, etc–Bacterial –Salmonella, Shigella, E. coli, Campylobacter, Clostridium difficile, etc–Fungal –histoplasmosis, etc–Protozoan –Cryptosporidium, Entamoeba histolytica -parasites like giardia |
|
|
Term
| Giardiasis is common in the midwest and can be contracted from |
|
Definition
| Contaminated water–Cool, clear stream–Well-water•Person to person–Kiddies in daycare centers |
|
|
Term
| Tumors of small intestine |
|
Definition
| •Adenocarcinoma•Neuroendocrine tumors (carcinoid)•Lymphoma•GIST (gastrointestinal stromal tumors)•Metastases from other sites] |
|
|
Term
| What are the symptoms of Acute Appendicitis? |
|
Definition
| •Pain starts periumbilically then localizes to the right lower quadrant•Nausea/vomiting, low-grade fever, and a mildly elevated peripheral white cell count |
|
|
Term
| How do you treat acute appendicitis? |
|
Definition
|
|
Term
| Appendicitis starts with acute inflammation and progresses to |
|
Definition
| serositis, inflammation of the serosa |
|
|
Term
| A Carcidnoid is a usually benign tumor often found in the tip of what organ? |
|
Definition
|
|
Term
|
Definition
| A dialated appendix filled with mucin, it is obstructed and can be from neoplastic process |
|
|
Term
| How many neurons are in the gut? |
|
Definition
|
|
Term
| GI microbiota outnumbers human cells to the point that we are only about ___ human |
|
Definition
|
|
Term
| The colon is involved in... |
|
Definition
| conservation of water, production and propulsion of feces. WHY DID SHE ADD A PICTURE?WHYYYYY? |
|
|
Term
| Normal colonic mucosa have crypts that are |
|
Definition
| long, straight, and parallel |
|
|
Term
| Normal colonic mucosa has... |
|
Definition
| About 1:1 ratio of crypts to lamina propria•About 50% cellularity of the lamina propria |
|
|
Term
| How many neurons are in the gut? |
|
Definition
|
|
Term
| GI microbiota outnumbers human cells to the point that we are only about ___ human |
|
Definition
|
|
Term
| Water must cross ________ and _________ to enter the capillaries of the superficial lamina propriaCollagen |
|
Definition
| the surface epithelium, collagen table |
|
|
Term
| Acute colitis can last... |
|
Definition
|
|
Term
| Chronic colitis can last... |
|
Definition
|
|
Term
|
Definition
| infectious, toxin related and ischemic |
|
|
Term
| The most common, but not most serious, form of colitis is |
|
Definition
|
|
Term
| In acute "self limited" colitis, you are likely to see lots of what sort of leukocyte in the crypt epithelium? |
|
Definition
|
|
Term
| What is an important morphological feature of acute "Self-limited" colitis? |
|
Definition
| crypt architecture is preserved |
|
|
Term
| Antibiotics can cause an overgrowth of what type of bacteria? |
|
Definition
|
|
Term
| Pseudomembranous colitis, often experience while on or following antibiotics, is cause by what toxin? |
|
Definition
|
|
Term
| Enterohemorrhagic E. coli -O157:H7 (verotoxin) exposure can be from |
|
Definition
| –fecal contamination–raw hamburger, sprouts, apples picked from ground in a pasture…. |
|
|
Term
| What is a morphological feature of pseuodomembranous colitis? |
|
Definition
| small, adherent yellow patches |
|
|
Term
| Ischemic Colitis, which is characterized by severe abdominal pain, nausea, vomiting, and bloody or melanotic stools is most common in what population? |
|
Definition
| Older patients, often with other vascular disease. |
|
|
Term
| Where can ISchemic colitis occur? |
|
Definition
| Anywhere from stomach to anus, but small intestine and colon are most frequent. |
|
|
Term
| These types of colitis are considered chronic colitis? |
|
Definition
| Inflammatory Bowel Disease (IBD)–Ulcerative colitis–Crohn’s disease•Microscopic colitis–Lymphocytic colitis–Collagenous colitis |
|
|
Term
| Irritable Bowel Syndrome (IBS), which is common and can be related to psychologic stressors, diet, and abnormal GI motility has what symptoms? |
|
Definition
| Chronic, relapsing abdominal pain, bloating, and changes in bowel habits• |
|
|
Term
| Idiopathic inflammatory bowel disease is a commonly used “umbrella” term that includes... |
|
Definition
| both ulcerative colitis and Crohn’s disease. |
|
|
Term
| Idiopathic inflammatory bowel disease is thought to result from a combination of... |
|
Definition
| –Defects in host interactions with intestinal microbiota–Intestinal epithelial dysfunction–Aberrant mucosal immune responses• |
|
|
Term
|
Definition
|
|
Term
| IBD that is diffuse, superficial and seen only in the colon can most likely be diagnosed as |
|
Definition
|
|
Term
|
Definition
| Focal (lymphoid aggregates and/or granulomas)•Transmural (mucosa through to serosa)•Anywhere in the GI tract (esp. ileum & colon) |
|
|
Term
| A feature of chronic colitis that distinguishes from acute is |
|
Definition
|
|
Term
| The number of neutrophils indicate what about the colitis? |
|
Definition
|
|
Term
| Ulcerative colitis always involves |
|
Definition
| the rectum and can involve confluent proximal colon |
|
|
Term
| Ulcerative colitis is a disease of which layers? |
|
Definition
|
|
Term
| What are the most commonly targeted areas in Chrohn's disease? |
|
Definition
|
|
Term
| What features of CD are all related to the transmural nature of the inflammation seen with CD? |
|
Definition
| Strictures, fistulas and adhesions |
|
|
Term
| A fissure ulcer extending into the submucosa might progress to be what? |
|
Definition
|
|
Term
| What are things that increase cancer risk in people with UC? |
|
Definition
| –more extensive disease–long duration ( > 8 years)–If primary sclerosing colangitis (PSC) also present |
|
|
Term
| Risk of cancer is moderate in what disease? |
|
Definition
|
|
Term
| Microscopic Colitis has what features |
|
Definition
| •Normal crypt architecture•Increased superficial chronic inflammation of the lamina propria•Increased numbers of intraepithelial lymphocytes•+/-thickened collagen table |
|
|
Term
| Diverticulosis(multiple diverticula) is present in what percent of those over 60 in the west? |
|
Definition
|
|
Term
|
Definition
| inflamed diverticulum and subject to perforation |
|
|
Term
|
Definition
| a projecting growth from a mucosal surface. |
|
|
Term
| Hyperplastic polyps are present in 15-30% of western populations where? |
|
Definition
|
|
Term
| Hyperplastic polyps are malignant or benign? |
|
Definition
|
|
Term
| Almost all colon cancers start from what? |
|
Definition
| A pre-cancerous colon polyp |
|
|
Term
| What does it mean when a polyp is said to be sessile? |
|
Definition
|
|
Term
| What type of polyp is small and sessile? |
|
Definition
|
|
Term
| How can you distinguish a hyperplastic polyp from a sessile serrated adenoma? |
|
Definition
| Serrated architecture extends to the base of the crypts with dilatation and branching of crypt base (inverted T-or L-shaped crypt) |
|
|
Term
| What large, sessile sort of polyp often found on the right-sided colon has malignant potential? |
|
Definition
|
|
Term
| The architecture of adenomas can be |
|
Definition
| tubular, tubolovillous, or villous |
|
|
Term
| By definition adenomas have what? |
|
Definition
| AT least low grade dysplasia and malignant potential |
|
|
Term
| What is the most common pathway to developing colon cancer? |
|
Definition
|
|
Term
| What sort of adenoma do the vast majority of colorectal cancers start with? |
|
Definition
|
|
